Botulinum toxin injected in small doses directly into muscle binds to the neuromuscular junction and inactivates it for approximately 3 months. This treatment has been demonstrated to be useful for strabismus and blepharospasm, but there has not been a complete understanding of its mechanism of action. Studies of utility of botulinum toxin have been carried out in spasmotic dysphonia and writer's cramp (and its varients such as pianist's cramp). Treatment appeared effective in both and a double-blind trial has been started for spasmotic dysphonia. Studies of physiology of the mode of action have been carried out in spasmotic dysphonia, writer's cramp, blepharospasm and hemifacial spasm. These studies show that the major effect of botulinum toxin is to weaken the muscle that is in spasm. Electromyogram (EMG) studies in writer's cramp, blepharospasm and hemifacial spasm show that spasms continue, but muscles are ineffective. No other changes in physiology were identified. In spasmotic dysphonia, there were a number of changes in physiology including reduction in spasms in non-injected muscles.